BIOL 121 Lecture Notes - Lecture 24: Tachycardia, Stroke Volume, Sympathetic Nervous System

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22 Jun 2020
School
Department
Course
Professor
Biol 121
Intro to Physiology
Summer 2018
Cardiac output- like ml per minute
CO= heart rate X stroke volume
Stroke volume- how much we pump out with each contraction
Increase of stroke volume, increase of heart rate
Not a good assumption at very high heart rates WHY?
High heart rate stroke volume goes down and CO is
affected
Heart rate is influenced by sympathetic (increase), parasympathetic
(decrease), hormone (increase)
Chemical messenger that decreases heart rate- acetylcholine
Stroke volume= EDV- ESV
From contract to relax- end systolic volume (ESV)
1. starling’s law- relationship that stretches has to volume. Increase
stretch, increase contraction strength
So bigger EDV, bigger stretch, increase contraction, increase stroke
volume, ESV decreases
2. contractility- sympathetic stimulation, hormones, increases
contraction….increase contraction strength but NOT due to stretch
(independent of stretch)
3. afterload- resistance in the artery, can be influenced by compliance
If increase afterload, flow goes down and ESV decrease
compliance-how easy it is to stretch something, stiffer takes more
pressure to stretch
From relax to contract- end diastolic volume (EDV)
These are all called preload
1. blood volume- more blood has ability to go to the heart, if you
don’t have enough it's hard to move it
2. skeletal muscle pump-when you contract skeletal muscle, it gets
bigger and the vein starts to collapse and blood is pressurized
toward the heart
venous return-trying to push blood out of veins into the
heart.
3. respiratory pump
4. venous vasoconstriction- increase flow, constrict vessel, increase
pressure and increase resistance
Caused by sympathetic nervous system
contractility, venous vasoconstriction and heart rate is influenced by a
sympathetic nervous system.
Cardiac output is flow, but not all flow is cardiac output
Arteriole is a small artery
Manipulates for pressure and flow
Local controls of blood flow (TABLE 12.7)
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Document Summary

Stroke volume- how much we pump out with each contraction. Increase of stroke volume, increase of heart rate. High heart rate stroke volume goes down and co is. Heart rate is influenced by sympathetic (increase), parasympathetic affected (decrease), hormone (increase) Chemical messenger that decreases heart rate- acetylcholine. From contract to relax- end systolic volume (esv) 1. starling"s law- relationship that stretches has to volume. So bigger edv, bigger stretch, increase contraction, increase stroke volume, esv decreases. 2. contractility- sympathetic stimulation, hormones, increases contraction . increase contraction strength but not due to stretch (independent of stretch) 3. afterload- resistance in the artery, can be influenced by compliance. If increase afterload, flow goes down and esv decrease. Compliance-how easy it is to stretch something, stiffer takes more pressure to stretch. From relax to contract- end diastolic volume (edv) 1. blood volume- more blood has ability to go to the heart, if you don"t have enough it"s hard to move it.

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